Dementia is a degenerative brain disorder identified clinically and more than fifty percents of people seventy and over are attacked by senile dementia. Average age of people in advanced country is already close to eighty, and thus the population of elderly people suffering from dementia is increasing, and the expenses for treating and caring of them reaches astronomical figures. In Korea, the population of dementia patients has increased suddenly as the average age of the population becomes higher, and thus the treatment and management of such patients are gathering urgency as social problems.
Upon pathological examination of dementia patients' cerebral cells and organs, plaque formed by accumulation of β-amyloid protein has been commonly observed. However, no one knows that such plaque works as pathogenic or be accumulated as products of pathogenesis. Forming of senile plaque in most of dementia patients and improving dementia symptoms decreasing of plaque are observed. Many researchers have looked for the cause of dementia and its treatment method, but they have not been revealed, yet.
In many countries, Research for treating method of the diseases of unknown cause with alternative medicines or medicinal foods has been conducted. Korean Pat. Application No.19330/2000 and International Pat. Application No. PCT/KR00/19330 by the present inventors, the content thereof being incorporated herein by reference, disclose hydroxy cinnamic acid derivatives or extract from Korean angelica root containing them, in which the compound is relatively simple 4-hydroxy-3-methoxy cinnamic acid (hereinafter, referred to as ferulic acid) having the following chemical structure. The excellent therapeutic effects of ferulic acid of dementia has been confirmed by an in vivo experiment, in which separated ferulic acid monomer is administered to mouse and then memory-retention ability of mouse is considerably increased. However, a biochemical mechanism of ferulic acid has not been revealed. 
Meanwhile, transthyretin protein, present in high concentrations in the blood, is known to be a representative plaque-forming protein, and is found in the cerebrospinal medulla of dementia patients, and is a material used for amyloidosis modelling.
The transthyretin exists in a stable tetrameric structure at physiological pH condition. However, the stable tetramer is destabilized by low pH, certain point mutations, and morphological changes induced by pressure, and can be further destabilized into monomeric form, the monomers then aggregating and thus forming plaque. That is, the decomposition process of transthyretin tetramers to monomers acts as a direct cause of senile plaque-formation. Furthermore, people afflicted by familial amyloid neuropathy characterized by unstable transthyretin tetramers of mutatant form can, in severe cases, lose their life.
Hence, the concentration of tetrameric transthyretin is in inverse proportion to formation of plaque. That is to say, transthyretin proteins constitute stable tetramer, and if stable tetramers are constituted, formation of plaque is markedly decreased.
In the blood, transthyretin are stabilized by forming conjugates with 25% of the total thyroid hormone thyroxine. Thyroxine is responsible for increasing the stability of transthyretin tetramers and preventing monomers, the cause of plaque, from being formed. However, even though thyroxine prevents formation of plaque, administration with excessive amounts may cause severe side effects.
X-ray crystalline structure of the transthyretin protein and thyroxine conjugate shows that, two thyroxine molecules are formed sandwiched form between two transthyretin dimers in the tetrameric structure, the dimers showing an enantiomeric image and constructing head to head or tail to tail. X-ray crystalline structures of the transthyretin proteins are observed in various compounds containing thyroxine.